Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Progesterone induction of 17 beta-hydroxysteroid dehydrogenase type 2 during the secretory phase occurs in the endometrium of estrogen-dependent benign diseases but not in normal endometrium
Autore:
Kitawaki, J; Koshiba, H; Ishihara, H; Kusuki, I; Tsukamoto, K; Honjo, H;
Indirizzi:
Kyoto Prefectural Univ Med, Dept Obstet & Gynecol, Kamigyo Ku, Kyoto 6028566, Japan Kyoto Prefectural Univ Med Kyoto Japan 6028566 Ku, Kyoto 6028566, Japan
Titolo Testata:
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
fascicolo: 9, volume: 85, anno: 2000,
pagine: 3292 - 3296
SICI:
0021-972X(200009)85:9<3292:PIO1BD>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RIBONUCLEIC-ACID; MENSTRUAL-CYCLE; ESTRADIOL DEHYDROGENASE; EXPRESSION; AROMATASE; RECEPTORS; LOCALIZATION; INVITRO; STROMA; CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Kitawaki, J Kyoto Prefectural Univ Med, Dept Obstet & Gynecol, Kamigyo Ku,465 Kajii Cho, Kyoto 6028566, Japan Kyoto Prefectural Univ Med 465 Kajii Cho Kyoto Japan 6028566
Citazione:
J. Kitawaki et al., "Progesterone induction of 17 beta-hydroxysteroid dehydrogenase type 2 during the secretory phase occurs in the endometrium of estrogen-dependent benign diseases but not in normal endometrium", J CLIN END, 85(9), 2000, pp. 3292-3296

Abstract

In the human endometrium, inactivation of 17 beta-estradiol to estrone is catalyzed by 17 beta-hydroxysteroid dehydrogenase type 2 (17 beta HSD2). Previous studies have shown that the 17 beta HSD2 activity in the endometriumis elevated during the secretory phase, as compared with the level during the proliferative phase, and that the elevation is in response to progesterone via the progesterone receptors. Recently, it has been demonstrated thataromatase cytochrome P450, the enzyme responsible for estrogen biosynthesis, is not present in the endometrium obtained from normal menstruating women with cervical cancer in situ showing no other gynecological disease (defined as "disease free"), but present in the endometrium obtained from patients with endometriosis, adenomyosis, and/or leiomyomas (defined as "diseased"). However, the previous 17 beta HSD studies have been performed without distinguishing between disease-free and diseased endometria. We, therefore, analyzed 17 beta HSD2 distinguishing between disease-free and diseased endometria. During the proliferative phase, the abundance of messenger RNA (mRNA) and activity of 17 beta HSD2 were comparable in both disease-free and diseased endometrium. However, during the secretory phase, while the abundance of mRNA and activity of 17 beta HSD2 increased 4- to B-fold in diseased endometrium, the 17 beta HSD2 remained unchanged in the disease-free endometrium. Kinetic studies showed that the K-m was identical among the four groups of endometria, suggesting that the elevation of 17 beta HSD2 simply resulted from increased mRNA transcription. Organ culture of proliferative endometria in the presence of progestins resulted in the stimulation of 17 betaHSD2 in diseased endometria via the progesterone receptors, whereas disease-free endometrium was not stimulated by progestins. These results suggest that the previous paradigm that 17 beta HSD2 activity in the endometrium iselevated during the secretory phase is confined to diseased endometrium but not to disease-free endometrium and that the estrogen metabolism is altered in the endometria of the patients with estrogen-dependent benign diseases.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 01:02:40